Smooth Muscle

Question 1

Smooth muscle cells

Answer 1

involuntary and electrically-coupled spindle like cells with gap junctions b/n each cell to ensure GRADUAL process in transmitting the impulse to the next cell

Question 2

Smooth muscle cell structure

Answer 2

• NO sarcomere (so can stretch to long lengths unrestricted)
• thin and thick filaments (NO troponin)
• side polar cross-bridges

Question 3

Varied tones of contraction

Answer 3

• actin-myosin ATPase hydrolyzes ATP SLOWER bc utilizes a different isoform of myosin, which saves energy
• can vary degree of tension over a range of functions
• never OFF, just more on/off depending on tension needs
• can stay contracted for a long time
  = way to save the MOST energy (LATCH)

Question 4

Why are the cross-bridges organized in a side polar fashion?

Answer 4

non-sarcomeric and no Z lines so the thin and thick filaments can slide over longer distances; myosin molecules assemble in a way that the cross-bridges are aligned differently so they can slide a longer distance and never encounter the wrong polarity cross-bridge

Question 5

Slow contraction velocity

Answer 5

• different isoform of myosin –> slower cross-bridge cycling but can still generate same if not MORE tension than skeletal muscle

Question 6

What must occur for myosin to be able to bind to actin in smooth muscle?

Answer 6

Myosin must be phosphorylated; the two cross-bridges stick togetherand get stuck on the shaft of thick filament

Question 7

Signaling Cascade for “Innervation” of smooth muscle

Answer 7

calcium crosses the plasma membrane after release from SR like membrane vesicles–> intracellular [ca] increases–> Ca binds to calmodulin (present in almost all cells) –> complex binds to myosin light chain kinase and phosphorylates myosin –> THEN myosin can interact w actin and the tension of the smooth muscle INCREASES
- calcium INDIRECTLY activates this signaling cascade

Question 8

How can smooth muscle relax?

Answer 8

• nonspecific phosphatases cleave the phosphate group from myosin to detach it from actin and the muscle can relax
• INHIBIT myosin light chain kinase
• DECREASE intracellular [Ca]

Question 9

Beta-adrenergic stimulation → cAMP rises → PKA activity increases → stimulates
removal of intracellular Ca2+ by vesicles – Does contraction Incr. or Decr.?

Answer 9

• decreased [Ca] will inhibit calmodulin from binding so MLCK won’t recognize the complex and it wont bind which is critical to phosphorylate myosin
  = DECREASED contraction

Question 10

Alpha-adrenergic stimulation → Rho-kinase activity increases → phosphorylates
myosin phosphatase → phosphatase activity decreases – Does contraction Incr.
or or Decr.?

Answer 10

phosphatase inactivated by getting phosphorylated so cannot cleave phosphate from myosin
= INCREASED contraction

Question 11

Extracellular nitric oxide concentration increases → cGMP increases → PKG activity increases → Rho
kinase activity decreases and/or phosphatase increases, inhibit Ca2+ entry into cell and stimulates
K+ efflux from cell leading to hyperpolarization – Does contraction Incr. or Decr.?

Answer 11

DECREASE

Question 12

cGMP

Answer 12

inhibits contraction

Question 13

Sildenafil Citrate (Viagra) → inhibits phosphodiesterase that degrades cGMP –
Does contraction Incr. or Decr.?

Answer 13

DECREASE contraction
- thus stimulating vasodilation (relaxation) and increased blood flow to a specific tissue

Question 14

Ultimately what dictates contraction time?

Answer 14

amount of contraction is a balance myosin
phosphorylation (allows myosin to bind to actin) vs. dephosphorylation (allows myosin to be removed from actin)

Question 15

Latch

Answer 15

Low energy cost tension maintenance
- specific to tonic muscles
- Low but super-basal levels of intracellular Ca2+ are present
- low but super-basal
levels of MLCK activity and myosin phosphorylation are maintained

Question 16

Stretch Activation of Smooth Muscle

Answer 16

non-specific & few stress-activated channels in smooth muscle so they do not generate enough of a potential diff to depolarize MEMBRANE enough BUT enough of a LOCAL change in membrane polarity to activate Voltage-gated channels and those channels bring about the depolarization